Can tomato juice be used for prophylaxis in recurrent stone formers?

binds calcium and forms a soluble salt. As a result, free ionic calcium concentration decreases.[1] Hess et al, demonstrated that citrate restored the inhibitory reactivity of TammHorsfall protein in stone formers.[2] Increase in the urine pH also increases ionization of uric acid into more soluble urate anions.[2,3] Citrate also prevents stone formation in other ways, like its ability to adhere on calcium oxalate and phosphate crystals to prevent agglomeration, nucleation, and crystal development; increases urine pH when oxidized into bicarbonate, slows renal citrate metabolism to interfere with citrate reabsorption and causes additional citraturic response.[4]

binds calcium and forms a soluble salt. As a result, free ionic calcium concentration decreases. [1] Hess et al, demonstrated that citrate restored the inhibitory reactivity of Tamm-Horsfall protein in stone formers. [2] Increase in the urine pH also increases ionization of uric acid into more soluble urate anions. [2,3] Citrate also prevents stone formation in other ways, like its ability to adhere on calcium oxalate and phosphate crystals to prevent agglomeration, nucleation, and crystal development; increases urine pH when oxidized into bicarbonate, slows renal citrate metabolism to interfere with citrate reabsorption and causes additional citraturic response. [4] In recurrent stone formers, potassium citrate is prescribed in doses of 1 meq/kg body weight, approximately 60 meq per day, as long-term prophylactic therapy. However, in medical management for stone prophylaxis patient compliance is generally low as potassium citrate has ulcerogenic potential and may cause gastrointestinal symptoms such as nausea, vomiting, diarrhea, and epigastric pain. These pharmacologic additions also bring about a serious financial burden. [3] The use of potassium citrate together with a potassium-holding diuretic such as triamterene, spironolactone, or amiloride may cause severe hypercalemia. [5] The high citric acid content of citrus fruits is known to have the potential to increase urine citrate excretion. Citrate that is consumed with the diet is absorbed immediately and almost completely (96 to 98%) through the gastrointestinal tract. More than 90% of the citrate that is absorbed is metabolized. Approximately 10% is excreted in urine without being metabolized. [1] In this study, authors have shown higher level of citrate in tomato as compared to citrus plants, which are natural sources of citrate. In addition, the lower level of oxalate as compared with that in citrus fruits is a noteworthy advantage. The high level of magnesium and low level of sodium and oxalate, particularly in fresh tomato juice, is also remarkable. In terms of calcium and pH levels, no

SUmmARy
In this study the authors have prospectively analyzed the results of 40 samples from tomato, orange, lemon, and mandarin juices. Ten samples of 100 ml were collected from four juice groups. Citrate, oxalate, calcium, phosphorus, magnesium, sodium, potassium, chloride, and pH levels were examined in all samples.
The same values were also examined after the samples were stored at 4°C for 1 week.
In fresh juice groups, in tomato juice statistically higher level of citrate (P < 0.001, P < 0.001, and P < 0.001, respectively), higher level of magnesium (P < 0.006, P < 0.009, P < 0.009), and lower level of sodium (P < 0.008, P < 0.009, P < 0.008) were found as compared to orange, lemon, and mandarin juices. No differences were found with regard to calcium, potassium, phosphorus, chloride, and pH in these juices.
Similarly, in stored juice groups, in tomato juice statistical higher level of citrate (P <0.001, P < 0.001, and P < 0.001, respectively), higher level of magnesium (P < 0.007, P < 0.009, P < 0.008), and lower level of sodium (P < 0.008, P < 0.011, P < 0.008) were found as compared to orange, lemon, and mandarin juices. No differences were found with regard to calcium, potassium, phosphorus, chloride, and pH in these juices.
In fresh juice group, statistically lower level of oxalate (P < 0.007, P < 0.008, P <0.006), were found in tomato juice as compared to orange, lemon, and mandarin juices. Higher level of oxalate was found in stored group as compared to fresh juice group (P <0.005).

COmmENTS
Citrate is one of the best known inhibitors of calciumbased stones. Citrate, with its strong anionic nature, significant differences were observed between tomato and citrus fruits. The amount of oxalate was shown to increase in stored tomato juice.
All above factors, that is higher citrate and magnesium levels as well as lower sodium and oxalate levels help in prevention of stone formation. Fresh tomato juice is well tolerated and inexpensive. The results of this study indicate that, following further human studies, fresh tomato juice may be recommended instead of pharmacologic potassium citrate for prophylactic purposes in mild to moderate hypocitraturic recurrent nephrolithiasis.
Interestingly, in India, there is widespread misconception among general population as well as among general practitioners that tomatoes are high in oxalate, and predispose to stone formation. This study convincingly demonstrates the truth to be just the opposite, and tomato juice may prove to be the treatment of choice in stone prevention.

SUmmARy
In this prospective trial, Pennesi et al, [1] randomized 100 children with vesicoureteral reflux (VUR) into a treatment arm, which received two years of oral sulfamethoxazole/ trimethoprim and a control arm that did not receive any chemoprophylaxis. Based on prior trials, a sample size of 48 was required for a 30% absolute risk difference. Analysis was done on an intention to treat basis. Children between the age of 1 day and 30 months at first episode of pyelonephritis were included. As Grade 1 would spontaneously resolve in the majority, and grade five has a high probability of being associated with renal dysplasia, only children who had grades 2-4 VUR were included. Voiding cystourethrography was performed in all, two months following the acute pyelonephritis. Renal ultrasound and DMSA scan were performed at six months. Although antibiotic prophylaxis was discontinued at two years in the intervention group, all subjects were followed up for a total period of four years. The results were quite an eye opener. Contrary to prior understanding, in the chemoprophylaxis group, there was a slightly higher risk, though not statistically significant, for developing pyelonephritis (RR 1.42 in the first year and 1.25 in the second year). 36% children in the prophylaxis group and 30% in the control group had at least one episode of pyelonephritis in the first two years. In the subsequent two years, both groups did not receive any prophylaxis. Only one in the intervention group and two in the control group developed pyelonephritis. However, it is noteworthy that all pyelonephritis episodes in the intervention arm were caused by multiresistant bacteriae, as opposed to sensitive organisms in the control group. There was no difference in the rate of renal scars or resolution of reflux between both groups. The authors conclude that antibiotic prophylaxis is ineffective either to prevent pyelonephritis recurrence, or to alter the course of the primary pathology.

COmmENTS
The cornerstone of management of VUR was hitherto thought to be antibiotic prophylaxis, on the premise that upper tract infection and renal damage could be prevented. Although we know from Hodson's water hammer theory that Scars could occur in sterile reflux, Edwards and Smellie [2] in their landmark publication in 1977 concluded that antibiotic prophylaxis had come to stay. Though surgical